摘要
目的:观察FAK、INTβ1在动脉粥样硬化(AS)斑块中的表达,探讨其在AS形成和发展过程中所起的作用。方法:将40只健康雄性新西兰白兔随机分为三组:(1)空白对照组(正常组)8只,喂基础饲料;(2)阳性对照组(模型组)16只,高脂高胆固醇饲料喂养;(3)木耳多糖组(预防组)16只,每天每兔给高脂高胆固醇饲料+5g木耳多糖喂养。12周末所有实验用兔麻醉处死,行主动脉粥样硬化病理形态学观察。通过HE染色、免疫组织化学染色对斑块内的病变进行定位、定量分析。结果:FAK、INTβ1在正常组呈弱阳性表达,而在模型组和预防组中血管内膜和中膜呈阳性表达。预防组与模型组对照的结果显示,FAK、INTβ1在预防组中的表达较模型组明显减少。结论:AS发生发展过程中存在FAK、INTβ1的异常表达。INTβ1-FAK信号转导通路可能在动脉粥样硬化发生发展过程中起重要作用。
Objective:This study is to investigate the expression of FAK and integrinβ1 in plaque of model group and normal group, to explore the relationship between FAK and integrinβ1 in the formation and progression of atherosclerosis. Methods:40 New Zealand white rabbits were randomly divided into 3 groups: normal group ( n = 8 ), model group ( n = 16), preventing group ( n = 16). Normal group always received normal chow;model group always received cholesterol chow ;preventing group always received cholestrol chow and 5g AAP. At the end of twelve week,all rabbits were killed to perform the pathologic examinations. In addition,the number of cell of FAK and integrinβ1 were analyzed by transmission microscopy and immunohistochemistry. Through HE, collagen changes were found increasing with the atherosclerotic lesion progression. Results: SABC immunohistochemistry analysis:The expression of the focal adhesion kinase(FAK)can be seen low expression of the FAK in nomal group rabbits. Rabbits of model group showed high expression of the FAK,the number of FAK in rabbits of preventing group decreased significantly. The results of INTβ1 just the same as the FAK. Conclusion:Abnormal expression of Integrinβ1 and FAK existed in AS. FAK signaling stimulated by Integrin clustering may play distinct roles in the course of AS.
出处
《牡丹江医学院学报》
2009年第5期1-4,共4页
Journal of Mudanjiang Medical University
基金
黑龙江省教育厅科学技术研究项目(11521335)